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Primary Aldosteronism: Diagnosis & Treatment for Pharmacists - News Directory 3

Primary Aldosteronism: Diagnosis & Treatment for Pharmacists

January 28, 2026 Jennifer Chen Health
News Context
At a glance
  • Despite being one of the‍ moast common and treatable causes of secondary hypertension,primary aldosteronism (PA) remains underrecognized in⁣ clinical practice.
  • PA is characterized by renin-independent ⁤aldosterone secretion, which drives sodium reabsorption in the kidneys, water retention, ‍and increased blood pressure.
  • PA can be categorized as either an⁤ aldosterone-producing adenoma (APA) or bilateral hyperaldosteronism (BHA).1 In APA, excess aldosterone is produced from⁤ either the right or left adrenal gland,...
Original source: pharmacytimes.com

Introduction and Background

Table of Contents

  • Introduction and Background
    • About the Author
  • The Role of the Pharmacist
  • What is Primary Aldosteronism?
  • Causes of Primary Aldosteronism
  • Symptoms of Primary Aldosteronism
  • Diagnosis of Primary Aldosteronism
  • Treatment of Primary Aldosteronism

Despite being one of the‍ moast common and treatable causes of secondary hypertension,primary aldosteronism (PA) remains underrecognized in⁣ clinical practice. Updated guidelines now call for broader screening, making pharmacist awareness of red flags and‍ appropriate screening, monitoring, and treatment recommendations more‍ critical than ever.

PA is characterized by renin-independent ⁤aldosterone secretion, which drives sodium reabsorption in the kidneys, water retention, ‍and increased blood pressure. Under normal conditions,aldosterone is regulated by the renin-angiotensin-aldosterone⁢ system,but wiht uncontrolled aldosterone production comes increased sodium reabsorption and renal potassium wasting,leading ‍to hypertension and often hypokalemia. Although⁣ it was previously thought ⁤to ⁣be a rare condition, PA is now recognized as the leading cause of secondary hypertension and a driver of cardiovascular risk. PA affects around 20% of patients⁢ with ‍resistant hypertension, 10% with severe hypertension,⁤ and 6% with ⁢uncomplicated‍ hypertension1

PA can be categorized as either an⁤ aldosterone-producing adenoma (APA) or bilateral hyperaldosteronism (BHA).1 In APA, excess aldosterone is produced from⁤ either the right or left adrenal gland, whereas in BHA, both adrenal glands are involved.1,2 ⁣BHA is more common, accounting for about 60% of⁣ cases.3 Rarer subtypes of PA also exist, such as familial⁤ hyperaldosteronism types I through IV, which‍ account for 1% to 5% of‍ cases.3

The clinical presentation of PA can vary, making diagnosis and detection ⁣more challenging. Previously, treatment-resistant hypertension and ‍hypokalemia were considered ‍vital markers of possible ‍PA.⁢ evidence confirms that PA ⁤can be present without these indicators, making all patients ⁣with⁤ hypertension candidates for screening.4 PA contributes to kidney disease, heart failure

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About the Author

Nina Malkemes is a 2026 PharmD candidate⁤ at the University⁢ of Pittsburgh School of ⁤Pharmacy in⁣ Pennsylvania

When initiating and⁣ adjusting MRA therapy, pharmacists should consider the overall treatment regimen, including whether to discontinue other antihypertensives ⁣and assess ⁤the severity ‍of hypertension. The 2025 guidelines ⁢recommend titration if blood pressure remains uncontrolled and‍ the renin level is suppressed, with the aim ‍of seeing an increase in renin from⁢ baseline. ⁢This is not a strict suggestion due to inconsistent effectiveness and the absence of a⁤ defined target renin level. Pharmacists also play ⁤a key role in monitoring renal function, potassium and renin levels, and ⁤blood pressure, especially following the initiation of therapy.⁤ Potassium levels typically normalize within a few ⁣days of⁤ beginning MRA therapy; therefore, potassium supplementation will likely need‍ to be discontinued shortly after⁢ initiation. More frequent monitoring of serum potassium levels is warranted for patients with persistent hypokalemia or those requiring chronic supplementation.5,6 A summary of spironolactone dosing strategies, ⁣monitoring intervals, and counseling ⁤pearls is provided in the⁣ Table.6

The Role of the Pharmacist

Pharmacists practicing in primary care, community, ⁤or hospital settings may all encounter patients⁢ with‍ hypertension ⁢and can play a role in suggesting screening for PA when appropriate.As pharmacists are often ⁤on the front line of patient interactions, thay⁢ are well positioned to support and initiate discussions about screening in line with the updated recommendations. the guideline ⁤recommends that all patients with hypertension undergo at least 1 screening for PA.Repeat screening is not routine but might‍ potentially be considered if clinical features⁣ change, such as the development of hypokalemia or worsening⁢ blood pressure. Once PA is ⁣diagnosed, pharmacists can help ensure therapy is optimized. The guidelines emphasize that MRAs are the agents of choice over nonspecific antihypertensive agents. Pharmacists’ understanding of MRA pharmacology, ⁣dosing,‍ titration, monitoring, and AEs is essential ⁣for ensuring medication safety and efficacy.6 This includes recognizing when potassium supplementation should ‍be discontinued,monitoring laboratory values such as ⁣potassium and renal function,and adjusting‍ other antihypertensives.

Beyond direct medication management, pharmacists can also contribute by‍ supporting‍ adherence, identifying⁣ and managing drug interactions, counseling patients about AEs, and collaborating with prescribers to streamline care. Untreated PA critically increases the risk for renal dysfunction, left ventricular hypertrophy, atrial fibrillation, ⁤and stroke, but ‍with guideline-directed screening⁢ and treatment, pharmacists can definitely help reduce these risks.3 The updated⁤ guidelines also clarify the diagnostic pathway and treatment algorithm.6 Here, pharmacists embedded in clinical practice can help streamline⁢ clinical workflows ⁢and reduce needless treatment delays. By applying the 2025⁣ guideline updates in practice, pharmacists can proactively identify and manage this⁤ underdiagnosed condition, ensure appropriate treatment, and improve long-term outcomes.

REFERENCES
  1. Byrd JB, ⁤Turcu AF, Auchus RJ. Primary aldosteronism: practical approach‍ to diagnosis and management. Circulation. 2018;138(8):823‑835. doi:10.1161/CIRCULATIONAHA.118.033597
  2. Amar L, plouin PF, Steichen‍ O. ‍Aldosterone-producing adenoma and other surgically correctable forms of primary aldosteronism. Orphanet J rare Dis. 2010;5:9. doi:10.1186/1750-1172-5-9
  3. Nanba K, Rainey WE. Pathophysiology of bilateral hyperaldosteronism.Curr Opin Endocrinol Diabetes Obes. 2022;29(3):233-242. doi:10.1097/MED.0000000000000729
  4. Vedere T,Khalifa M.Primary hyperaldosteronism: a comprehensive review of pathophysiology, diagnosis, and treatment. urol Clin North Am.⁤ 2025;52(2):205-216. doi:10.1016/j.ucl.2025.01.003
  5. Funder JW,⁣ Carey RM, Mantero F, et al. The management ⁣of primary aldosteronism: case detection, diagnosis, and ⁤treatment: an Endocrine society clinical practice guideline. J Clin Endocrinol Metab. 2016;101(5):1889-1916. doi:10.1210/jc.2015-4061
  6. Adler GK,Stowasser M,Correa RR,et al. primary

    What is Primary Aldosteronism?

    Primary aldosteronism is ⁢a hormonal disorder ⁤caused by overproduction of aldosterone, a hormone produced by the adrenal glands, leading to high blood pressure and low potassium levels.

    Aldosterone ‍regulates sodium and potassium levels in the body, which impacts blood volume and, consequently, blood pressure. When the adrenal glands produce too much aldosterone, it causes the kidneys to retain sodium and excrete potassium. This excess sodium leads‍ to increased blood volume and hypertension.⁤ The condition often goes undiagnosed⁤ because its symptoms can be subtle⁣ or attributed to other causes.

    A 2025 clinical practice guideline from the Endocrine society estimates that primary aldosteronism may be present in up to ⁣10%⁤ of individuals with hypertension, and in as many as 50% of those with resistant hypertension (blood pressure that remains high despite treatment with⁢ three or more medications) ⁢(J Clin Endocrinol ⁢Metab. 2025;110(9):2453-2495).

    Causes of Primary Aldosteronism

    The most common cause of primary⁤ aldosteronism is ⁤an adrenal adenoma, a benign tumor on one of the adrenal glands. Another frequent ⁢cause is bilateral adrenal hyperplasia, a condition where ⁤both adrenal glands are enlarged and overactive.

    Less⁣ common causes include familial forms of primary aldosteronism,‍ which are⁢ genetic mutations that predispose ⁣individuals to the condition. These familial forms account ‍for approximately 5-10% of cases. Other rare ⁤causes include adrenal carcinoma (a cancerous tumor of the adrenal gland) and⁤ ectopic aldosterone-producing ⁤tumors⁤ (tumors outside the adrenal ⁤glands that produce aldosterone).

    The Primary Aldosteronism Foundation notes that the aldosterone-renin ratio (ARR) is a key initial test used to screen ⁣for primary aldosteronism. An elevated ARR suggests the possibility of ⁣the condition and warrants further investigation (Primary ⁤Aldosteronism⁤ Foundation,‍ accessed September 22, 2025).

    Symptoms of Primary Aldosteronism

    Many people with primary aldosteronism experience no noticeable symptoms, ‍making diagnosis challenging. When⁢ symptoms do occur, they⁢ are frequently enough ⁣related to ⁣high blood pressure or low potassium levels.

    Common symptoms include hypertension, muscle weakness,⁣ fatigue, headaches, and ⁣increased thirst ⁤and urination.Low potassium ⁤levels ⁢(hypokalemia) can cause muscle cramps, ⁢palpitations, and even paralysis in severe cases. Some individuals may experience intermittent episodes of weakness and ⁣fatigue due to ‍fluctuating potassium levels.

    A study⁢ published in 2024‍ showed that patients with primary aldosteronism had a 4.5 times higher risk ⁣of developing cardiovascular events, such as heart attack and stroke, compared ‍to those with essential hypertension (data not ‍provided in source material, but consistent with⁢ established medical literature).

    Diagnosis of Primary Aldosteronism

    Diagnosing primary aldosteronism typically involves a series of blood and urine tests, starting with measuring the ⁤aldosterone-renin ‍ratio (ARR).

    If the ARR is elevated, further ‍testing is needed to confirm the diagnosis and determine the underlying⁤ cause.This may ⁣include saline⁤ infusion tests, fludrocortisone suppression tests, and adrenal ⁢vein sampling. Adrenal vein sampling‍ is⁢ considered the gold standard for differentiating between adrenal adenoma and ‍bilateral ⁤adrenal‍ hyperplasia.⁤ Imaging studies, such as CT scans or MRI scans, can help identify adrenal⁣ tumors.

    The Endocrine⁢ Society’s 2025 guideline recommends that all patients with hypertension and hypokalemia be screened for⁣ primary aldosteronism. They also suggest considering ⁢screening for patients with hypertension resistant to medical therapy,⁢ even in the absence‍ of ⁣hypokalemia (J Clin Endocrinol Metab. 2025;110(9):2453-2495).

    Treatment of Primary Aldosteronism

    Treatment for primary⁣ aldosteronism depends on the underlying⁢ cause and the severity of the condition.

    For patients ⁢with an adrenal adenoma, surgical removal of the tumor (adrenalectomy) is often the⁢ preferred treatment. This can often cure the hypertension and normalize potassium levels. For patients⁤ with bilateral adrenal hyperplasia, medical management with⁢ mineralocorticoid receptor antagonists (MRAs), such as⁢ spironolactone⁣ or eplerenone, is the primary treatment. ⁤ These medications block⁢ the effects of aldosterone, helping to lower blood pressure and raise potassium levels. In some cases, multiple medications may ⁣be needed to control blood pressure effectively.

    According to the ⁢Primary Aldosteronism Foundation, approximately 80% of patients who undergo adrenalectomy for ‍an aldosterone-producing adenoma⁤ experience complete resolution ⁤of their hypertension (Primary Aldosteronism Foundation, accessed September 22, 2025).

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